Acute Respiratory Failure

NUR 409/Fall2014-2015

What is respiratory Failure???

Acute Respiratory Failure

Not a disease but a conditionResult of one or more diseases involving the lungs or other body systems

Acute Respiratory Failure “Inability of the lung to meet the metabolic demands of the body. This can be from failure of tissue oxygenation and/or failure of CO2

homeostasis.” A sudden and life-threatening deterioration in pulmonary gas exchange, resulting in carbon dioxide retention and inadequate oxygenation.

Acute Respiratory Failure

Results from inadequate gas exchange◦Insufficient O2 transferred to the blood Hypoxemia

◦Inadequate CO2 removal Hypercapnia

QuestionQuestion

Which of the following findings indicates acute respiratory failure?– A. PaO2 of 60 mm Hg, PaCO2 of 45 mm Hg, arterial

pH less than 7.35– B. PaO2 of 55 mm Hg, PaCO2 of 50 mm Hg, arterial

pH less than 7.35– C. PaO2 of 70 mm Hg, PaCO2 of 45 mm Hg, arterial

pH less than 7.45

Answer

B. PaO2 of 55 mm Hg, PaCO2 of 50 mm Hg, arterial pH less than 7.35

Rationale: Acute respiratory failure is defined as a PaO2 of 55 mm Hg or less, a PaCO2 greater than 50 mm Hg, and an arterial pH less than 7.35. This definition is valid only in cases in which baseline ABG values are assumed to be normal.

Respiration is gas exchange between the organism and its environment. Function of respiratory system is to transfer O2 from atmosphere to blood and remove CO2 from blood.

Clinically Respiratory failure is defined as PaO2 <60 mmHg while breathing air, or a PaCO2 >50 mmHg.

Acute respiratory failure is defined as a PaO2 of 50 mm Hg or less, a PaCO2 greater than 50 mm Hg, and an arterial pH less than 7.35

Definition

Acute Respiratory Failure Control of Respirations

◦ Involuntary control mediated in respiratory center in brain stem (pons & medulla)

◦ Change in carbon dioxide and oxygen levels in blood◦ Hypercapnia: Increase of carbon dioxide-stimulus to breath◦ Hypoxemia: decrease in oxygen in blood can cause

increase in respirations but less effective◦ Hypoventilation – slow, shallow breathing causes carbon

dioxide to build in blood

Regulation of Respiration

Respiratory Centera. Pons= controls rate & depth of inspiration.b. Medulla Oblongata= control rhythm of respiration.** ChemoreceptorCenter-medulla oblongata: Monitor arterial blood indirectly by sensing

changes in the PH of CSF. Sensitive to very small changes in PH. Increased levels of CO2= low PH==

stimulates respiratory center to increase depth & rate of ventilation.

Regulation of Respiration

Peripheral: aortic bodies & carotid bodies)

Located in aortic bodies of aortic arch & carotid bodies at bifurcation of the carotids.

Primarily sensitive to changes in O2 levels in the arterial blood, do detect changes in CO2 & PH.

As PaO2 & PH decrease= peripheral chemo-receptors stimulate respiratory center to increase ventilation.

Regulation of RespirationPeripheral: aortic bodies & carotid bodies)

Peripheral chemoreceptors not sensitive as central chemoreceptors PaO2 must drop to approximately 60 mmHg before the peripheral chemoreceptors have much influence on ventilation.

It become the major stimulus to ventilation when center chemoreceptors are reset by chronic hypoventilation.

A 70-year-old man was admitted to the intensive care unit with acute hypoxemic respiratory failure. 48 hours earlier, he underwent a surgical resection of the lower lobe of the left lung for stage IIIB adenocarcinoma of the lung. During the 6-hour operation, he received a total fluid infusion of 5.5 L (including 3 units of packed red blood cells). The cumulative fluid infusion given during the peri-operative period (during surgery and the first 24 hours post-op) was 8.0 L with a net negative 0.7L. While the patient was in the recovery room, the endotracheal tube was removed without complications, and he transferred to the ward a few hours later.  Approximately 36 hours later, dyspnea and hypoxemia were noted, and after 4 hours of continued hypoxemia, the trachea was inutbated to facilitate mechanical ventilation.

Case Presentation

Pathophysiology

ARF

ARF

FIO2

Ventilation without

perfusion(deadspace

ventilation)

Diffusion abnormality

Perfusion without

ventilation (shunting)

Hypoventilation

Normal

FIO2

Ventilation without

perfusion(deadspace

ventilation)

Diffusion abnormality

Perfusion without

ventilation (shunting)

Hypoventilation

Normal

Perfusion without ventilation (Shunting) Intra-cardiac

◦ Any cause of right to left shunt eg Fallot’s, Eisenmenger

Intra-pulmonary◦ Pneumonia◦ Pulmonary oedema◦ Atelectasis◦ Collapse◦ Pulmonary haemorrhage or contusion

Perfusion without ventilation (shunting)Intra-pulmonary Small airways occluded ( e.g asthma, chronic

bronchitis)

Alveoli are filled with fluid ( e.g pulm edema, pneumonia)

Alveolar collapse ( e.g atelectasis)

FIO2

Ventilation without

perfusion(deadspace

ventilation)

Diffusion abnormality

Perfusion without

ventilation (shunting)

Hypoventilation

Normal

V/Q mismatch:

Dead space ventilation

Alveoli that are normally ventilated but poorly perfused

Anatomic dead space

Gas in the large conducting airways that does not come in contact with the capillaries e.g pharynx

V/Q mismatch:Dead space ventilation

Physiologic dead space

Alveolar gas that does not equilibrate fully with capillary blood

Dead space vantilation

DSV increase:◦Alveolar-capillary interface destroyed e.g emphysema

◦Blood flow is reduced e.g CHF, PE◦Overdistended alveoli e.g positive- pressure ventilation

FIO2

Ventilation without

perfusion(deadspace

ventilation)

Diffusion abnormality

Perfusion without

ventilation (shunting)

Hypoventilation

Normal

Diffusion abnormality:

Less common

Abnormality of the alveolar membrane or a reduction in the number of capillaries resulting in a reduction in alveolar surface area

Causes include:◦ Acute Respiratory Distress Syndrome◦ Fibrotic lung disease

Table 33-2 Conditions That Impair Pulmonary Gas Exchange

FIO2

Ventilation without

perfusion(deadspace

ventilation)

Diffusion abnormality

Perfusion without

ventilation (shunting)

Hypoventilation

Normal

Brainstem

Spinal cordNerve rootAirway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause ventilatory disturbance

Brainstem

Spinal cordNerve rootAirway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause ventilatory disturbance

Brainstem

Spinal cordNerve rootAirway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause ventilatory disturbance

Brainstem

Spinal cordNerve rootAirway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause ventilatory disturbance

Brainstem

Spinal cordNerve rootAirway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause ventilatory disturbance

Brainstem

Spinal cordNerve rootAirway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause ventilatory disturbance

Brainstem

Spinal cordNerve rootAirway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause ventilatory disturbance

Classification of Respiratory Failure

Fig. 68-2

Classification of Respiratory Failure

Acute Respiratory Failure Type I respiratory failure, in which processes that

impair oxygen transfer in the lung cause hypoxaemia (acute or hypoxaemic respiratory failure)

Type II respiratory failure, in which inadequate ventilation leads to retention of CO2, with hypercarbia and hypoxaemia (chronic, ventilatory or hypercapnic respiratory failure).

‘mixed’ respiratory failure, in which there is a combination of type I and type II respiratory failure (acute-on-chronic respiratory failure).

HYPOXEMIC RESPIRATORY FAILURE (TYPE I)

The principal problem in type I acute respiratory failure is the inability to achieve adequate oxygenation, as evidenced by a PaO2 of 50 mm Hg or less and a PaCO2 of 40 mm Hg or less.

HYPOXEMIC RESPIRATORY FAILURE(TYPE I)

PaO2 <60mmHg with normal or low PaCO2 normal or high

Most common form of respiratory failure Lung disease is severe to interfere with

pulmonary O2 exchange, but over all ventilation is maintained

Physiologic causes: V/Q mismatch and shunt

HYPOXEMIC RESPIRATORY FAILURE(TYPE I)

Causes The most common cause of hypoxemia

is ventilation–perfusion mismatch. Right-to-left shunt Alveolar hypoventilation. FiO2

HYPOXEMIC RESPIRATORY FAILURE(TYPE I)

Caused by a disorder of heart, lung or blood. Etiology easier to assess by CXR abnormality:

- Normal Chest x-ray Cardiac shunt (right to left)

Asthma, COPD Pulmonary embolism

- Focal infiltrates on CXR Atelectasis Pneumonia

HYPOXEMIC RESPIRATORY FAILURE(TYPE I)

Diffuse infiltrates on CXR Cardiogenic Pulmonary Edema Non cardiogenic pulmonary edema

(ARDS) Interstitial pneumonitis or fibrosis Infections

Diffuse pulmonary Infiltrates intrapulmonary shuntunt

Hypercapnic Respiratory Failure (Type II)

Is the result of inadequate alveolar ventilation and is characterized by marked elevation of carbon dioxide with relative preservation of oxygenation. Hypoxemia results from reduced alveolar pressure of oxygen (PAO2) and is proportionate to hypercapnia.

Hypercapnic Respiratory Failure (Type II)

Acute Arterial pH is low Causes

- sedative drug over dose- acute muscle weakness such as

myasthenia gravis- severe lung disease:

alveolar ventilation can not be maintained (i.e. Asthma or pneumonia)

Hypercapnic Respiratory Failure (Type II)

Decreased ventilatory drive.respiratory muscle fatigue or failure.

increased work of breathing.

Hypercapnic Respiratory Failure (Type II)

Decreased ventilatory drive:◦ medications/drugs (narcotics, benzodiazepines,barbiturates, alcohol), brainstem lesions,

hypothyroidism,◦ morbid obesity, and sleep apnea

respiratory muscle fatigue or failure:◦ neuromuscular dysfunction (amyotrophic lateral

sclerosis, Guillain-Barré syndrome, myasthenia gravis, muscular dystrophy, and polymyositis.

Hypercapnic Respiratory Failure (Type II)

increased work of breathing:◦COPD (increased dead space) or asthma (elevated airway resistance), and it may also result from thoracic abnormalities (restriction on lungs) such as pneumothorax, rib fractures, or pleural effusions

Hypercapnic Respiratory Failure (Type II)

PaCO2 >50 mmHg Hypoxemia is always present pH depends on level of HCO3

HCO3 depends on duration of hypercapnia Renal response occurs over days to weeks

Combined hypoxemic and hypercapnic Respiratory Failure Acute respiratory failure develops as a

consequence of a combined inadequate alveolar ventilation and abnormal gas transport.

Commonly seen in asthmatic exacerbations, emphysema complicated by a lower respiratory tract infection, severe pneumonia, pulmonary edema, and pulmonary embolism

Acute Respiratory Failure

Patient Presentation

Acute Respiratory Failure Presentation of acute respiratory failure

may vary, depending on the underlying disease, precipitating factor(s), and the degree of hypoxemia, hypercapnia, or acidosis.

The classic symptom of hypoxemia is dyspnea.

The cardinal symptoms of hypercapnia are dyspnea and headache.

Neurological◦Restlessness◦Anxiety◦Confusion◦Headache◦Lethargy to coma

Cardiovascular

◦Tachycardia◦Elevated blood pressure early◦Eventual hypotension◦Skin Hypercarbnia - warm and wet Hypoxemia -cold and wet

Respiratory

◦Increased rate and depth (hyperpnea)

◦Dyspnea ◦Cyanosis.◦Paradoxical breathing

Renal

◦Decreas UOP◦Erythropoietin release with hypoxemia

◦Excretion of H+ and retention of HCO3

- with respiratory acidosis

Gastrointestinal

◦Decreased bowel sounds◦Reduced gastric pH with tissue hypoxia

Acute Respiratory Failure Assessment Careful history Physical Examination Tests

◦ABGs, CXR, PFTs, CT, thoracentesis, ECG

Acute Respiratory Failure Management: Therapy is directed toward correcting the

cause and alleviating the hypoxia and hypercapnia.

Endotracheal intubation and mechanical ventilation may be lifesaving ◦ Correction of gases, oxygen therapy ◦ Reversal of any narcotics◦ Possible mechanical ventilation

Acute Respiratory Failure Management Principles: Hypoxemia may cause death in RF Primary objective is to reverse and

prevent hypoxemia Secondary objective is to control PaCO2

and respiratory acidosis Treatment of underlying disease Patient’s CNS and CVS must be monitored

and treated

Acute Respiratory Failure- O2 therapy Supplemental O2 therapy essential titration based on SaO2, PaO2 levels and PaCO2 Goal is to prevent tissue hypoxia Tissue hypoxia occurs (normal Hb & C.O.)

- venous PaO2 < 20 mmHg or SaO2 < 40%

- arterial PaO2 < 38 mmHg or SaO2 < 70% Increase arterial PaO2 > 60 mmHg(SaO2 >

90%) or venous SaO2 > 60% O2 dose either flow rate (L/min) or FiO2 (%)

Acute Respiratory Failure- O2 Therapy O2 toxicity:

- very high levels(>1000 mmHg) CNS toxicity and seizures - lower levels (FiO2 > 60%) and longer exposure: - capillary damage, leak and pulmonary fibrosis - PaO2 >150 can cause retrolental fibroplasia - FiO2 35 to 40% can be safely tolerated indefinitely

CO2 narcosis: - PaCO2 may increase severely to cause respiratory

acidosis, somnolence and coma - PaCO2 increase secondary to combination of

a) abolition of hypoxic drive to breathe b) increase in dead space

Acute Respiratory Failure- MV

Non invasive with a mask Invasive with an endobronchial tube MV can be volume or pressure cycled for

hypercapnia: - MV increases alveolar ventilation and lowers

PaCO2, corrects pH - rests fatigues respiratory muscles

For hypoxemia: - O2 therapy alone does not correct hypoxemia caused by shunt- Most common cause of shunt is fluid filled or collapsed alveoli (Pulmonary edema)

Acute Respiratory distress Syndrome

ARDS

Acute inflammatory response to some “trigger”

Mediators released Alveolar capillary injury is the result

ARDS Hypoxia that persists even when oxygen is

administered at 100% Decreased pulmonary compliance Dyspnea Noncardiac-associated bilateral pulmonary

edema Dense pulmonary infiltrates seen on x-ray

Question

Is the following statement true or false?

Acute respiratory distress syndrome (ARDS) is typically caused by left ventricular failure with acute pulmonary edema.

Answer

False

Rationale: The pulmonary edema is noncardiogenic.

Definitions of ARDS and ALI

Statistics Related to ARDS/ALI

Approximately 190,600 cases of ARDS occur each year in the United States.

Results in 74,500 deaths Greatest risk for development:

◦ Sepsis◦ Age older than 65 years◦ Severe acute illness◦ Preexisting chronic disorder

Physiological Effects

Impaired oxygenation Pulmonary vasoconstriction

◦ Pulmonary hypertension◦ Reduced blood flow

Impaired ventilation Decrease lung compliance and increase

airway resistance Fluid-filled alveoli Alveolar collapse Bronchoconstriction

Direct Injury

Indirect Injury

Pathological Changes

SIRS Definition

Pathophysiology

Inciting event Inflammatory mediators

◦ Damage to microvascular endothelium◦ Damage to alveolar epithelium◦ Increased alveolar permeability results in alveolar

edema fluid accumulation

Pathophysiology Pathological changes in lung vascular

tissue, lung edema, and impaired gas exchange are hallmarks of pathophysiology.

Pathological changes are directly related to a cascade of events resulting from release of cellular and biochemical mediators

Pathophysiology Interstitial/alveolar edema

Severe hypoxemia◦ due to intra-pulmonary shunt (V/Q = 0)◦ shunt ~ 25% - 50%

Increased airway resistance

Pathophysiology High ventilatory demands

◦ high metabolic state◦ decreased lung compliance

Pulmonary HTN◦ neurohumoral factors, hypoxia, edema

ARDS Stages

Stage 1 ARDS

Increased dyspnea and tachypnea initially Few radiographic changes Rapid progress of severity symptoms

◦ Cyanosis, coarse bilateral crackles◦ Patchy infiltrates on CXR

Dry cough may be present.

Stage 2 ARDS

Mediator-induced disruption of vascular bed Increased interstitial and alveolar edema

◦ Increasingly permeable to proteins “Exudative stage” Hypoxia-resistant supplemental oxygen Worsening PaO2:FiO2 ratio

Stage 3 ARDS

“Proliferative” stage Develops 2nd to 10th day after injury Hemodynamic instability, generalized

edema, hypoxemia, nosocomial infections Decreased lung volumes Diffuse interstitial markings

Stage 4 ARDS

“Fibrotic” stage Develops after 10 days Increases PaCO2

Multiorgan involvement, SIRS Progressive lung fibrosis

◦ Ventilation management difficulties◦ Increased airway pressures◦ Pneumothoraces

Assessment

Physical Examination

Hypotension, tachycardia Hyperthermia or hypothermia Tachypnea, dyspnea Restlessness and agitation

◦ Lethargy ominous sign Hypoxia and decreases in oxygen saturation Crackles

ARDS-Diagnostic Onset ~ 24-48 hours after trigger

◦ Dyspnea◦ Tachypnea due to reduced compliance◦ Cough◦ Tachycardia◦ Other s/s due to hypoxemia◦ Adventitious breath sounds

Continuous - rhonchi, wheezed Discontinuous - crackles/rales

ARDS-Diagnostic Acute dyspnea/tachypnea

◦ rales/rhonchi/wheezing

Resistant hypoxemia◦ PaO2/FIO2 < 150 – 200 mmHg

CXR◦ diffuse, bilateral infiltrates

No evidence of LV failure◦ (PAWP < 18 mmHg)

ARDS-clinical manifestation

Stage I (first 12hrs): Dyspnea, Tachypnea, restlessness, normal

CXR Respiratory alkalosis. Use of accessory muscles. Elevated PAP, normal PAWP.

ARDS-clinical manifestation

Stage II (24hrs): Client increases respiratory rate & uses

accessory muscles. Client becomes cyanotic, dyspnic (severe)

and develops crackles. Increase agitation & restlessness. X-ray show alveolar infiltration. Decrease SaO2 despite O2 therapy. Metabolic acidosis. Elevated PAP & Normal PAWP.

ARDS-clinical manifestation

Stage III (2-3 days) Continued resp failure results (worsening hypoxemia),

hemodynamic instability & mental confusion. Systemic Inflammatory Syndrome presentation. Increase interstitial & alveolar inflammatory exudates. X-ray shows diffused alveolar infiltration & decreased

lung volume. Decrease GI motility. Generalized edema. Poor skin integrity. Increased WBC, decrease Hb & Platelets. Abnormal clotting factors.

ARDS-clinical manifestation

Stage IV (>10 days). Multiple organ failure or single respiratory system

involvement with gradual improvement over time.Decrease UO, GI motility, impaired coagulation. Difficulty maintaining adequate oxygenation. Worsening hypoxemia & hypercapnia. Sepsis, pneumonia, & multi-system involvement. X-ray shows persistent infiltrates & new

pneumonic infiltrates & Pneumothorax. Thickening of interstitial wall with fibrosis,

macrophages, & remodling of arterioles.

Arterial Gas Analysis

Refractory hypoxemia Persistently low SaO2

Early—decreased PaCO2

◦ Respiratory alkalosis Hypercarbia develops later.

◦ Respiratory acidosis

Radiographic Studies

Chest radiographic◦ Patchy bilateral alveolar infiltrates◦ Progress to diffuse infiltrates, consolidations, and

air bronchograms◦ Pneumothoraces

ARDS-Diagnostic Clinical

Evidence CXR PaO2 PaCO2 % shunt

None Normal 80-100 35-45 3-5%

Mild to moderate tachypnea

Minimal/No change

70-80 25-35 10-15%

Severe tachypnea

Bilateral infiltrates

50-60 20-35 20-30%

End stage Opacification 35-50 30-60 30-50%

ARDS-Diagnostic

ARDS-Diagnostic

Intrapulmonary Shunt

Perfusion without ventilation (shunt) Ventilation without perfusion (dead space) Combination of both ARDS more than 15% shunt PaO2: FiO2 ratio

◦ Normal > 300◦ 200 associated with 15% to 20% intrapulmonary

shunt◦ 100 associated with more than 20% intrapulmonary

shunt

Question

Which of the following would be the correct PaO2/FiO2 ratio with the following?– PaO2 80 %

– FiO2 40%– A. 350– B. 250– C. 125– D. 200

Answer

D. 200

Rationale: 80 ÷ 0.40 = 200– Remember to use the decimal point for FiO2%.

ARDS-Diagnostic Physicians diagnose ARDS when:

• A person suffering from severe infection or injury develops breathing problems.

• A chest x-ray shows fluid in the air sacs of both lungs.

• Arterial blood gases show a low level of oxygen in the blood

• Other conditions that could cause breathing problems have been ruled out.

ARDS-Diagnostic

ARDS can be confused with other illnesses that have similar symptoms. The most important is congestive heart failure. In congestive heart failure, fluid backs up into the lungs because the heart is weak and cannot pump well. However, there is no injury to the lungs in congestive heart failure. Since a chest x-ray is abnormal for both ARDS and congestive heart failure, it can be difficult to tell them apart.

ARDS-Management

Monitoring:◦Respiratory◦Hemodynamic◦Metabolic◦Infections◦Fluids/electrolytes

ARDS-Management

Endotracheal intubation and mechanical ventilation with positive end-expiratory pressure or continuous positive airway pressure

Drug therapy Nutrition therapy; fluid therapy Case management

ARDS-Management History to identify contributing factors for

ARDS (behavioral, social, medications). Treat cause if possible, for example give

antibiotics. Intubation & mechanical ventilation with O2 set

to maintain PO2 >60mmHg, & O2Sat is 90% or more.

Low tidal volume. High PEEP. Inverse ration of ventilation 2:1or 3:1. Monitor fluid balance (I& O), ABGs level & VS. Nutrition enteral or TPN:35-45 kcal/day. Prevent complications (DVT, Nosocomial

infection, skin breakdown). Positioning (frequent changed, prone), Sedation to promote comfort & reduce

respiratory efforts.

Oxygenation and Ventilation

Refractory hypoxemia hallmark of ARDS Goal to optimize oxygen delivery

◦ Arterial oxygenation◦ Hemoglobin◦ Cardiac output

Fluid management Positive inotropic agents and

vasoconstrictors

Ventilation and oxygenation

Optimizing oxygen delivery:DO2 = Q X CaO2

DO2 = Q X (1.34 X Hb X SaO2) X 10Q = cardiac outputCaO2 = arterial oxygen contentNormal DO2: 520-570 ml/min/m2

Mechanical Ventilation

Lung protective ventilation strategies◦ Limits ventilator-associated lung injury (VALI)

Includes◦ Low tidal volumes◦ PEEP◦ Limit plateau pressures to 30 cm H2O

Ventilation Strategies

Permissive hypercapnia Pressure-controlled ventilation Inverse-ratio ventilation Airway pressure release ventilation

Ventilation and Oxygenation

PEEP Effects Increases transpulmonary distending

pressure◦ Displaces edema fluid into interstitium◦ Decreases atelectasis◦ Decrease in right to left shunt◦ Improved compliance◦ Improved oxygenation

Positioning

Frequent position changes HOB elevated to prevent VAPS Prone positioning

◦Improves gas exchange

Pharmacological Therapy

Antibiotics, if indicated Bronchodilators and mucolytics IV corticosteroids Nitric oxide Sedation Neuromuscular blocking agents

Pharmacologic Support Meds to treat ARDS may include:

◦ Anti-inflammatories Decrease inflammation

◦ Vasodilators Improve ventilation/perfusion ratios

◦ Surfactant & Beta-Agonists Decrease surface tension of alveoli

◦ Cytokine Inhibitors Decrease inflammatory cytokines

Nutritional Support

Enteral feeding benefits Balanced caloric, protein, carbohydrate, and

fat intake Usually require 35 to 45 kcal/kg/d High carbohydrates avoided to prevent

excess carbon dioxide production Antioxidants and omega-3 fatty acids

Nursing Actions

Prevention of VAP◦Hand washing◦Line care◦Oral care

Nursing Actions Paralysis

◦ Minimize O2 demand and improve ventilator synchrony

◦ Commonly used agents Propofol, fentanyl, and midazolam

◦ Daily sedation vacations allow neuro assessment and decrease vent days

Nursing Actions

Positioning◦Prone positioning can improve oxygenation

◦Helps recruit uninjured alveoli

ARDS-Management

Complications

Sepsis/SIRS Volutrauma

◦ Pneumothorax◦ Pneumomediastinum

VAP Immobility DVT/PE